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Vitamin A Deficiency Has Different Effects on Immunoglobulin A Production and Transport During Influenza A Infection in BALB/c Mice^1,2,

Department of International Health, School of Public Health ^* Department of Microbiology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294

We examined the effect of advanced vitamin A deficiency (serum retinol 0.35 µmol/L, with weight gain significantly lower than in controls with free access to food) on the secretory immunoglobulin A (IgA) response to a mild, upper respiratory tract infection with influenza A virus in BALB/c mice. Mice fed a vitamin A-deficient or control diet were infected intranasally at 11 to 12 wk of age. The influenza-specific salivary IgA response was lower in the vitamin A-deficient mice (0.11 ± 0.13% of total IgA 4 wk after infection) than in controls with free access to food (2.73 ± 1.86%, P < 0.0001). In a separate experiment, the response of vitamin A-deficient mice (0.42 ± 1.51%) was also lower than that of pair-fed controls (3.43 ± 4.76%, P < 0.0001). In addition, fewer influenza A-specific IgA-secreting plasma cells were found in the salivary glands of vitamin A-deficient mice (geometric mean 3.0%) than in controls with free access to food or in pair-fed controls (geometric mean 8.7%, P < 0.0001). Although the pathogen-specific IgA response was decreased, vitamin A-deficient mice had a significantly higher concentration of total salivary IgA (31.9 ± 15.9 mg/L) than did the pair-fed controls (14.3 ± 8.4 mg/L, P < 0.0001). Northern blot analysis of salivary gland RNA revealed that these vitamin A-deficient mice also had greater levels of mRNA of the polymeric immunoglobulin receptor (pIgR), which transports IgA across mucosal surfaces (pIgR: ß-actin mRNA ratio = 7.8 ± 0.8), than did pair-fed control mice (3.7 ± 0.4, P = 0.0001). These data demonstrate that vitamin A deficiency has contrasting effects on the secretory IgA response to influenza infection, with a principal effect being a decrease in the pathogen-specific response.

KEY WORDS: • vitamin A • immunoglobulin A • influenza A • polymeric immunoglobulin receptor • mice

¹ We acknowledge the support of research grant RO1 HD30293 from the National Institutes of Health.

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom correspondence and reprint requests should be addressed.

Manuscript received 29 April 1996. Revision accepted 28 August 1996.

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